【摘要】 目的　探讨花生四烯酸是否能诱导小鼠成纤维细胞L92 9凋亡及其可能机制。方法　用四甲基偶氮唑盐(MTT)法和乳酸脱氢酶 (LDH)释放率测定细胞存活率及损伤程度 ,比色法测定细胞脂质过氧化产物丙二醛 (MDA)含量 ,Hoechst 3 3 2 58染色观察凋亡细胞核形态变化 ,DNA琼脂糖凝胶电泳检测DNA降解情况。结果　L92 9细胞在低浓度花生四烯酸 (40～ 160 μmol·L- 1)作用 2 4h后 ,细胞存活率明显下降 ,LDH释放率和细胞MDA含量显著增加 (P <0 .0 1)。经 160 μmol·L- 1花生四烯酸处理后的L92 9细胞呈现典型的凋亡核固缩表现。琼脂糖凝胶电泳显示DNA凋亡梯带。结论　高浓度花生四烯酸 (80～ 160 μmol·L- 1)能诱导小鼠成纤维细胞L92 9凋亡 ,其中促脂质过氧化作用可能是一个关键因素更多还原

【Abstract】 ObjectiveTo observe whether arachidonic acid (AA) could induce apopt osis in mice fibroblast cell line L929 and the potential mechanism involved.MethodsThe viability and damaged degree of L929 were monitor ed by MTT and the release of lactate dehydrogenase (LDH).Lipid peroxidation in L 929 was measured as malondialdehyde (MDA) content by colorimetric assay.Hoechst 33258 staining was used to observe AA-induced morphological changes.Agarose g el electrophoresis w as used to detect DNA fragmentation.ResultsTreatment of L929 cell with AA for 24?h,in the range of 40～160?μmol·L -1 ,caused a great decrease in cel l survival and increased MDA contents and the release of LDH simultaneously ( P <0.01).Cells treated by 160?μmol·L -1 AA showed typical morphological changes o f apoptosis.A “ladder” pattern representing fragmentation of DNA into oligonuc leosome length fragments was observed 24?h after AA treatment.ConclusionHigher concentration of arachidonic acid(80～160?μmol·L -1 ) induced apoptosis in mice fibro blast cell line L929.Lipid peroxidation might play a role in AA-induced apoptos is in L929 cells.更多还原